Poly (ADP-Ribose) Polymerase-1 causes mitochondrial damage and neuron death mediated by Bnip3, J Neurosci. 2014 Nov 26;34(48):15975-87

Bhattacharyya, Pallabi

doi:10.5214/ans.0972.7531.220309

Cited by 3 publications

(2 citation statements)

References 3 publications

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“…Overexpression of PARP-1 is the most critical step to initiate parthanatos, during which PARP-1 synthesises PAR using NAD + as substrate in the presence of ATP 29 . Parthanatos is reported that it is related to a variety of diseases, such as diabetes, inflammation, Brain trauma and so on 30 , 31 . An important feature is the dependence on the PARP-1 protein, and previous study found that Cd treatment of renal tubular epithelial cells could increase the expression of PARP proteins significantly 32 .…”

Section: Discussionmentioning

confidence: 99%

PARP-1 overexpression contributes to Cadmium-induced death in rat proximal tubular cells via parthanatos and the MAPK signalling pathway

Luo

Yuan

et al. 2017

Sci Rep

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Parthanatos is a newly discovered form of PARP-1-dependent programmed cell death. It has been reported to play an important role in several cancer or tumour cells; however, few studies have been performed in normal cells. Cadmium is a highly toxic pollutant and is reported to induce autophagy and apoptosis in multiple cell types. Although cadmium toxicity induces cell death, the underlying mechanism is not fully understood. Therefore, in this study we aimed to investigate the mechanism of Cadmium -induced cell damage using rat proximal tubular cell line NRK-52E and primary rat proximal tubular (rPT) cells. Our results indicated that parthanatos and the MAPK signalling pathway contribute to Cadmium-induced cell death, and that oxidative stress and mitochondrial damage play key roles in this process. In addition, parthanatos with oxidative stress has a synergistic effect on apoptosis, and JNK1/2 and p38 contribute to parthanatos.

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Section: Discussionmentioning

confidence: 99%

PARP-1 overexpression contributes to Cadmium-induced death in rat proximal tubular cells via parthanatos and the MAPK signalling pathway

Luo

Yuan

et al. 2017

Sci Rep

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“…However, there are also studies showing that FoxO3a positively regulates: i. NGF withdrawal-induced cell death by binding to BIM (a BH3-only member of the BCL-2 family) promoter and activating its transcription in superior cervical ganglia sympathetic neurons 36 ; ii. Poly (ADP-ribose) polymerase-1 (PARP1) -induced mitochondrial dysfunction and neuronal cell death by enhancing association of FoxO3A with Bcl2/adenovirus E1B 19 kDa interacting protein (Bnip3- a pro-apoptotic member of the BH3-only subfamily of Bcl-2 proteins) promoter, increasing its transcription and elevating its mitochondrial immunoreactivity in primary mouse brain cortical neuronal cultures 37 ; iii. Leptin regulation of brain-adipose feedback axis in energy metabolism by FoxO3a binding to cystathionine-β-synthase (CBS) promoter and then enhanced CBS protein expression in primary neonatal rat thalamus neuronal cultures and the hypothalamus of Sprague-Dawley rats 38 .…”

Section: Discussionmentioning

confidence: 99%

FoxO3a suppresses neuropeptide W expression in neuronal cells and in rat hypothalamus and its implication in hypothalamic-pituitary-adrenal (HPA) axis

Yan¹,

Wang²,

Li³

et al. 2020

Int. J. Biol. Sci.

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FoxO3a, a forkhead family member of transcription factors, is involved in the regulation of cell metabolism, proliferation, differentiation and apoptosis. However, whether FoxO3a participates in the regulation of glucocorticoids induced-hypothalamic-pituitary-adrenal (HPA) dysfunction is still unknown. Our present results indicate that dexamethasone(DEX) increased FoxO3a expression in PC12 and hypothalamic neuronal cultures in correlation to reduced expression of NPW, a process that could be blocked by GR2 antagonist. DEX restrained the phosphorylation of Akt and FoxO3a, but not ERK1/2 phosphorylation, resulting with FoxO3a nuclear localization. Overexpression of FoxO3a inhibited NPW expression, while FoxO3a knockdown by siRNA had the opposite effect. The regulatory region of NPW promoter contains multiple FoxO3a binding sites, and FoxO3a bonding to these sites inhibited its transcriptional activity. In a rat model, chronic administration of corticosterone reduced animals' body weight and sucrose consumption and caused stress-depression like behavior. Corticosterone treatment induced a marked increase in FoxO3a levels, while decreased the expression of NPW protein in the hypothalamus. Immunofluorescent double labeling demonstrated that FoxO3a and NPW were collocated in the hypothalamus. Taken together, these data indicate that NPW is a new direct downstream target gene of FoxO3a. FoxO3a suppressed the transcription of NPW and modulated glucocorticoids-induced HPA dysfunction by directly regulating the expression of NPW. Thus, present findings suggest that FoxO3a and NPW may be potential therapeutic targets for endocrine and psychiatric disorders.

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The Commonalities in Bacterial Effector Inhibition of Apoptosis

Robinson

2016

Trends in Microbiology

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Poly (ADP-Ribose) Polymerase-1 causes mitochondrial damage and neuron death mediated by Bnip3, J Neurosci. 2014 Nov 26;34(48):15975-87

Cited by 3 publications

References 3 publications

PARP-1 overexpression contributes to Cadmium-induced death in rat proximal tubular cells via parthanatos and the MAPK signalling pathway

PARP-1 overexpression contributes to Cadmium-induced death in rat proximal tubular cells via parthanatos and the MAPK signalling pathway

FoxO3a suppresses neuropeptide W expression in neuronal cells and in rat hypothalamus and its implication in hypothalamic-pituitary-adrenal (HPA) axis

The Commonalities in Bacterial Effector Inhibition of Apoptosis

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